Direct comparison between regional cerebral metabolism in progressive supranuclear palsy and Parkinson's disease
Identifieur interne : 000713 ( Istex/Corpus ); précédent : 000712; suivant : 000714Direct comparison between regional cerebral metabolism in progressive supranuclear palsy and Parkinson's disease
Auteurs : Reinoud C. Klein ; Bauke M. De Jong ; Joeke J. De Vries ; Klaus L. LeendersSource :
- Movement Disorders [ 0885-3185 ] ; 2005-08.
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- KwdEn :
Abstract
The differentiation between progressive supranuclear palsy (PSP) and Parkinson's disease (PD) may be difficult, especially in the early stages of disease. Positron emission tomography potentially provides a tool for making such a distinction. To identify key features in the spatial distributions of cerebral glucose metabolism, 18F‐fluorodeoxyglucose (FDG) measurements of 10 patients with probable or possible PSP were directly compared with those of 9 PD patients. This analysis was done with statistic parametric mapping. After normalization of global brain uptake, in PSP, relative uptake of FDG was reduced in the caudal (motor) part of the anterior cingulate gyrus (Brodmann's area BA 24; P < 0.05, corrected for multiple comparisons). At a lower threshold, an additional decrease was present in the dorsal mesencephalon. In PD, relative hypometabolism was seen in extrastriate visual, ventrolateral temporal, posterior parietal, and orbitofrontal regions. Only reduction in the right fusiform gyrus and the lateral extrastriate visual cortex reached statistical significance. We concluded that particularly the reduction of medial frontal metabolism may be a valuable diagnostic imaging parameter in distinguishing PSP from PD. For PD, a possible association between occipitotemporal FDG decrease and vulnerability to hallucinations is suggested. © 2005 Movement Disorder Society
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DOI: 10.1002/mds.20493
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De Jong</name><affiliation><mods:affiliation>Department of Neurology, University Hospital Groningen, The Netherlands</mods:affiliation></affiliation><affiliation><mods:affiliation>PET Center, University Hospital Groningen, The Netherlands</mods:affiliation></affiliation></author><author><name sortKey="De Vries, Joeke J" sort="De Vries, Joeke J" uniqKey="De Vries J" first="Joeke J." last="De Vries">Joeke J. De Vries</name><affiliation><mods:affiliation>Department of Neurology, University Hospital Groningen, The Netherlands</mods:affiliation></affiliation></author><author><name sortKey="Leenders, Klaus L" sort="Leenders, Klaus L" uniqKey="Leenders K" first="Klaus L." last="Leenders">Klaus L. 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Klein</name><affiliation><mods:affiliation>Department of Neurology, University Hospital Groningen, The Netherlands</mods:affiliation></affiliation></author><author><name sortKey="De Jong, Bauke M" sort="De Jong, Bauke M" uniqKey="De Jong B" first="Bauke M." last="De Jong">Bauke M. De Jong</name><affiliation><mods:affiliation>Department of Neurology, University Hospital Groningen, The Netherlands</mods:affiliation></affiliation><affiliation><mods:affiliation>PET Center, University Hospital Groningen, The Netherlands</mods:affiliation></affiliation></author><author><name sortKey="De Vries, Joeke J" sort="De Vries, Joeke J" uniqKey="De Vries J" first="Joeke J." last="De Vries">Joeke J. De Vries</name><affiliation><mods:affiliation>Department of Neurology, University Hospital Groningen, The Netherlands</mods:affiliation></affiliation></author><author><name sortKey="Leenders, Klaus L" sort="Leenders, Klaus L" uniqKey="Leenders K" first="Klaus L." last="Leenders">Klaus L. 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Positron emission tomography potentially provides a tool for making such a distinction. To identify key features in the spatial distributions of cerebral glucose metabolism, 18F‐fluorodeoxyglucose (FDG) measurements of 10 patients with probable or possible PSP were directly compared with those of 9 PD patients. This analysis was done with statistic parametric mapping. After normalization of global brain uptake, in PSP, relative uptake of FDG was reduced in the caudal (motor) part of the anterior cingulate gyrus (Brodmann's area BA 24; P < 0.05, corrected for multiple comparisons). At a lower threshold, an additional decrease was present in the dorsal mesencephalon. In PD, relative hypometabolism was seen in extrastriate visual, ventrolateral temporal, posterior parietal, and orbitofrontal regions. Only reduction in the right fusiform gyrus and the lateral extrastriate visual cortex reached statistical significance. We concluded that particularly the reduction of medial frontal metabolism may be a valuable diagnostic imaging parameter in distinguishing PSP from PD. For PD, a possible association between occipitotemporal FDG decrease and vulnerability to hallucinations is suggested. © 2005 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Reinoud C. Klein MD</name><affiliations><json:string>Department of Neurology, University Hospital Groningen, The Netherlands</json:string></affiliations></json:item><json:item><name>Bauke M. de Jong MD, PhD</name><affiliations><json:string>Department of Neurology, University Hospital Groningen, The Netherlands</json:string><json:string>PET Center, University Hospital Groningen, The Netherlands</json:string></affiliations></json:item><json:item><name>Joeke J. de Vries MD</name><affiliations><json:string>Department of Neurology, University Hospital Groningen, The Netherlands</json:string></affiliations></json:item><json:item><name>Klaus L. Leenders MD, PhD</name><affiliations><json:string>Department of Neurology, University Hospital Groningen, The Netherlands</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>progressive supranuclear palsy</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Parkinson's disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>PET</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>FDG</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>SPM</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>medial frontal metabolism</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>hallucination</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>cingulate gyrus</value></json:item></subject><language><json:string>eng</json:string></language><abstract>The differentiation between progressive supranuclear palsy (PSP) and Parkinson's disease (PD) may be difficult, especially in the early stages of disease. Positron emission tomography potentially provides a tool for making such a distinction. To identify key features in the spatial distributions of cerebral glucose metabolism, 18F‐fluorodeoxyglucose (FDG) measurements of 10 patients with probable or possible PSP were directly compared with those of 9 PD patients. This analysis was done with statistic parametric mapping. After normalization of global brain uptake, in PSP, relative uptake of FDG was reduced in the caudal (motor) part of the anterior cingulate gyrus (Brodmann's area BA 24; P > 0.05, corrected for multiple comparisons). At a lower threshold, an additional decrease was present in the dorsal mesencephalon. In PD, relative hypometabolism was seen in extrastriate visual, ventrolateral temporal, posterior parietal, and orbitofrontal regions. Only reduction in the right fusiform gyrus and the lateral extrastriate visual cortex reached statistical significance. We concluded that particularly the reduction of medial frontal metabolism may be a valuable diagnostic imaging parameter in distinguishing PSP from PD. 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Box 30.001, 9700 RB Groningen, The Netherlands</p></note><affiliation>Department of Neurology, University Hospital Groningen, The Netherlands</affiliation><affiliation>PET Center, University Hospital Groningen, The Netherlands</affiliation></author><author><persName><forename type="first">Joeke J.</forename><surname>de Vries</surname><roleName type="degree">MD</roleName></persName><affiliation>Department of Neurology, University Hospital Groningen, The Netherlands</affiliation></author><author><persName><forename type="first">Klaus L.</forename><surname>Leenders</surname><roleName type="degree">MD, PhD</roleName></persName><affiliation>Department of Neurology, University Hospital Groningen, The Netherlands</affiliation></author></analytic><monogr><title level="j">Movement Disorders</title><title level="j" type="sub">Official Journal of the Movement Disorder Society</title><title level="j" type="abbrev">Mov. 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Positron emission tomography potentially provides a tool for making such a distinction. To identify key features in the spatial distributions of cerebral glucose metabolism, 18F‐fluorodeoxyglucose (FDG) measurements of 10 patients with probable or possible PSP were directly compared with those of 9 PD patients. This analysis was done with statistic parametric mapping. After normalization of global brain uptake, in PSP, relative uptake of FDG was reduced in the caudal (motor) part of the anterior cingulate gyrus (Brodmann's area BA 24; P < 0.05, corrected for multiple comparisons). At a lower threshold, an additional decrease was present in the dorsal mesencephalon. In PD, relative hypometabolism was seen in extrastriate visual, ventrolateral temporal, posterior parietal, and orbitofrontal regions. Only reduction in the right fusiform gyrus and the lateral extrastriate visual cortex reached statistical significance. We concluded that particularly the reduction of medial frontal metabolism may be a valuable diagnostic imaging parameter in distinguishing PSP from PD. For PD, a possible association between occipitotemporal FDG decrease and vulnerability to hallucinations is suggested. © 2005 Movement Disorder Society</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>progressive supranuclear palsy</term></item><item><term>Parkinson's disease</term></item><item><term>PET</term></item><item><term>FDG</term></item><item><term>SPM</term></item><item><term>medial frontal metabolism</term></item><item><term>hallucination</term></item><item><term>cingulate gyrus</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>Article category</head><item><term>Research Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2004-06-01">Received</change><change when="2004-12-14">Registration</change><change when="2005-08">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/F2F637EC05B7BC0B812D9C560DADEE4938A1A5E5/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Wiley Subscription Services, Inc., A Wiley Company</publisherName><publisherLoc>Hoboken</publisherLoc></publisherInfo><doi registered="yes">10.1002/(ISSN)1531-8257</doi><issn type="print">0885-3185</issn><issn type="electronic">1531-8257</issn><idGroup><id type="product" value="MDS"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="MOVEMENT DISORDERS">Movement Disorders</title><title type="subtitle">Official Journal of the Movement Disorder Society</title><title type="short">Mov. 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Box 30.001, 9700 RB Groningen, The Netherlands</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:MDS.MDS20493.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="4"></count><count type="tableTotal" number="3"></count><count type="referenceTotal" number="46"></count><count type="wordTotal" number="6291"></count></countGroup><titleGroup><title type="main" xml:lang="en">Direct comparison between regional cerebral metabolism in progressive supranuclear palsy and Parkinson's disease</title><title type="short" xml:lang="en">Regional Cerebral Metabolism in PSP and PD</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Reinoud C.</givenNames><familyName>Klein</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1 #af2" corresponding="yes"><personName><givenNames>Bauke M.</givenNames><familyName>de Jong</familyName><degrees>MD, PhD</degrees></personName><contactDetails><email>b.m.de.jong@neuro.azg.nl</email></contactDetails></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Joeke J.</givenNames><familyName>de Vries</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Klaus L.</givenNames><familyName>Leenders</familyName><degrees>MD, PhD</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="NL" type="organization"><unparsedAffiliation>Department of Neurology, University Hospital Groningen, The Netherlands</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="NL" type="organization"><unparsedAffiliation>PET Center, University Hospital Groningen, The Netherlands</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">progressive supranuclear palsy</keyword><keyword xml:id="kwd2">Parkinson's disease</keyword><keyword xml:id="kwd3">PET</keyword><keyword xml:id="kwd4">FDG</keyword><keyword xml:id="kwd5">SPM</keyword><keyword xml:id="kwd6">medial frontal metabolism</keyword><keyword xml:id="kwd7">hallucination</keyword><keyword xml:id="kwd8">cingulate gyrus</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>The differentiation between progressive supranuclear palsy (PSP) and Parkinson's disease (PD) may be difficult, especially in the early stages of disease. Positron emission tomography potentially provides a tool for making such a distinction. To identify key features in the spatial distributions of cerebral glucose metabolism, <sup>18</sup>F‐fluorodeoxyglucose (FDG) measurements of 10 patients with probable or possible PSP were directly compared with those of 9 PD patients. This analysis was done with statistic parametric mapping. After normalization of global brain uptake, in PSP, relative uptake of FDG was reduced in the caudal (motor) part of the anterior cingulate gyrus (Brodmann's area BA 24; <i>P</i> < 0.05, corrected for multiple comparisons). At a lower threshold, an additional decrease was present in the dorsal mesencephalon. In PD, relative hypometabolism was seen in extrastriate visual, ventrolateral temporal, posterior parietal, and orbitofrontal regions. Only reduction in the right fusiform gyrus and the lateral extrastriate visual cortex reached statistical significance. We concluded that particularly the reduction of medial frontal metabolism may be a valuable diagnostic imaging parameter in distinguishing PSP from PD. For PD, a possible association between occipitotemporal FDG decrease and vulnerability to hallucinations is suggested. © 2005 Movement Disorder Society</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><!--Version 0.6 générée le 4-12-2015--><mods version="3.6"><titleInfo lang="en"><title>Direct comparison between regional cerebral metabolism in progressive supranuclear palsy and Parkinson's disease</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Regional Cerebral Metabolism in PSP and PD</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Direct comparison between regional cerebral metabolism in progressive supranuclear palsy and Parkinson's disease</title></titleInfo><name type="personal"><namePart type="given">Reinoud C.</namePart><namePart type="family">Klein</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, University Hospital Groningen, The Netherlands</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Bauke M.</namePart><namePart type="family">de Jong</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Neurology, University Hospital Groningen, The Netherlands</affiliation><affiliation>PET Center, University Hospital Groningen, The Netherlands</affiliation><description>Correspondence: Department of Neurology, University Hospital Groningen, P.O. Box 30.001, 9700 RB Groningen, The Netherlands</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Joeke J.</namePart><namePart type="family">de Vries</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, University Hospital Groningen, The Netherlands</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Klaus L.</namePart><namePart type="family">Leenders</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Neurology, University Hospital Groningen, The Netherlands</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre authority="originalCategForm">article</genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2005-08</dateIssued><dateCaptured encoding="w3cdtf">2004-06-01</dateCaptured><dateValid encoding="w3cdtf">2004-12-14</dateValid><copyrightDate encoding="w3cdtf">2005</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">4</extent><extent unit="tables">3</extent><extent unit="references">46</extent><extent unit="words">6291</extent></physicalDescription><abstract lang="en">The differentiation between progressive supranuclear palsy (PSP) and Parkinson's disease (PD) may be difficult, especially in the early stages of disease. Positron emission tomography potentially provides a tool for making such a distinction. To identify key features in the spatial distributions of cerebral glucose metabolism, 18F‐fluorodeoxyglucose (FDG) measurements of 10 patients with probable or possible PSP were directly compared with those of 9 PD patients. This analysis was done with statistic parametric mapping. After normalization of global brain uptake, in PSP, relative uptake of FDG was reduced in the caudal (motor) part of the anterior cingulate gyrus (Brodmann's area BA 24; P < 0.05, corrected for multiple comparisons). At a lower threshold, an additional decrease was present in the dorsal mesencephalon. In PD, relative hypometabolism was seen in extrastriate visual, ventrolateral temporal, posterior parietal, and orbitofrontal regions. Only reduction in the right fusiform gyrus and the lateral extrastriate visual cortex reached statistical significance. We concluded that particularly the reduction of medial frontal metabolism may be a valuable diagnostic imaging parameter in distinguishing PSP from PD. For PD, a possible association between occipitotemporal FDG decrease and vulnerability to hallucinations is suggested. © 2005 Movement Disorder Society</abstract><subject lang="en"><genre>Keywords</genre><topic>progressive supranuclear palsy</topic><topic>Parkinson's disease</topic><topic>PET</topic><topic>FDG</topic><topic>SPM</topic><topic>medial frontal metabolism</topic><topic>hallucination</topic><topic>cingulate gyrus</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title><subTitle>Official Journal of the Movement Disorder Society</subTitle></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><subject><genre>article category</genre><topic>Research Article</topic></subject><identifier type="ISSN">0885-3185</identifier><identifier type="eISSN">1531-8257</identifier><identifier type="DOI">10.1002/(ISSN)1531-8257</identifier><identifier type="PublisherID">MDS</identifier><part><date>2005</date><detail type="volume"><caption>vol.</caption><number>20</number></detail><detail type="issue"><caption>no.</caption><number>8</number></detail><extent unit="pages"><start>1021</start><end>1030</end><total>10</total></extent></part></relatedItem><identifier type="istex">F2F637EC05B7BC0B812D9C560DADEE4938A1A5E5</identifier><identifier type="DOI">10.1002/mds.20493</identifier><identifier type="ArticleID">MDS20493</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2005 Movement Disorder Society</accessCondition><recordInfo><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin><recordContentSource>WILEY</recordContentSource></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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